scholarly journals The biological implications of the "alcoholic hyaline" phenomenon

Kanzo ◽  
1980 ◽  
Vol 21 (11) ◽  
pp. 1431-1436
Author(s):  
SAMUEL W. FRENCH
Keyword(s):  
1977 ◽  
Vol 123 (4) ◽  
pp. 351-358 ◽  
Author(s):  
SHOZO NAKAMURA ◽  
YOSHIAKI TAKEZAWA ◽  
TAKASHI SATO ◽  
TATSUYA AIKAWA ◽  
KIYOSHI KERA

1982 ◽  
Vol 17 (5) ◽  
pp. 434-440
Author(s):  
Takeshi Okanoue ◽  
Tadao Okuno ◽  
Ongyoku Ou ◽  
Jun Yoshida ◽  
Takeshi Ogasawara ◽  
...  

1959 ◽  
Vol 34 (5) ◽  
pp. 261-263 ◽  
Author(s):  
B. J. P. Becker ◽  
D. S. F. Treurnich

1968 ◽  
Vol 46 (3) ◽  
pp. 463-473 ◽  
Author(s):  
W. Stanley Hartroft ◽  
Eduardo A. Porta

The concept of the prevention of fatty livers and cirrhosis by lipotropic factors and protein led to the notion that the latter might also be capable of affording protection against similar liver damage frequently seen in alcoholic man. The relevant literature, which had been published before the first investigations in this area were undertaken in Professor Best's department in 1949, is briefly cited. Developments in this field then utilized three approaches: experiments in which alcohol when administered in the drinking water supplied 27% of calories (Best), experiments with a completely fluid diet which supplied 36% of calories as alcohol (Lieber), and experiments in which an ethanol–sucrose mixture (Porta) in place of drinking water supplied 40–60% of calories as alcohol, with the remainder provided by semisynthetic diets. Most of the results obtained from these investigations did not support the concept of a direct hepatotoxic action of alcohol. Finally, evidence is presented that alcohol did not prevent regression of established cirrhosis in rats if they were treated by a "super diet" which contained abundant lipotropes and protein. Mallory bodies (alcoholic hyaline) formed in liver cells of alcohol-fed rats if basal diets were inadequate; the same structures appeared in rats fed certain other inadequate diets even without alcohol, and their development was prevented in rats consuming large amounts of alcohol if the basal diets were suitably fortified. The mitochondrial nature of these bodies was demonstrated. It is concluded that even large intakes of alcohol for weeks or months by rats do not injure their livers if the accompanying diet is suitably designed.


Micron (1969) ◽  
1980 ◽  
Vol 11 (2) ◽  
pp. 195-196
Author(s):  
N. Benson ◽  
R. Munn ◽  
J. Beirne ◽  
S. Akeda ◽  
S.W. French

1978 ◽  
Vol 37 (5) ◽  
pp. 582 ◽  
Author(s):  
M. Akima ◽  
S. Nonaka ◽  
S. Ichimori ◽  
A. Aoyama ◽  
N. Fukunaga

2021 ◽  
Vol 22 (3) ◽  
pp. 22-26
Author(s):  
V. S. Paukov ◽  
◽  
Y. A. Kirillov ◽  
I. A. Chernov ◽  
◽  
...  

The authors consider alcohol disease (AD) as an independent disease, the pathogenesis of which passes 3 stages: episodic alcohol intoxication, drunkenness and alcoholism. In the last 2 stages, severe changes in organs and tissues develop. In this case, Mallory bodies appear in the liver, which is considered to be a marker of chronic alcohol intoxication (CAI). They are observed in most patients with alcoholism and very rarely in those suffering from alcoholism. The authors believe that the alcoholic hyaline Mallory bodies, appearing in the liver and other organs in CAI, is an autoantigen to which the body responds with an autoimmune inflammatory response that is not curable. Therefore, drunkenness, in which there are no Mallory bodies, is curable when alcohol is consumed within the basal metabolism of the liver and treated by therapists, and the treatment of alcoholism is futile. Therefore, the problem of CAI can be solved only with the active treatment of the stage of drunkenness by therapists with the participation of psychiatrists.


1977 ◽  
Vol 3 ◽  
pp. 145-150 ◽  
Author(s):  
Ellen Borenfreund ◽  
Paul J. Higgins ◽  
Aaron Bendich

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